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psychiatry > therapy > Flashcards

therapy Flashcards

1
Q

what is CBT particularly good at treating

A

depression, anxiety, phobias, OCD, PTSD

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2
Q

what is the main principle of CBT

A

How our thoughts relate to our feelings and behaviour

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3
Q

what focus CBT focus on

A

Focus on here and now, problem focused, goal- orientated

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4
Q

in what ways can CBT be given

A

Individual, group, self-help book or computer programme

Therapist helps client:

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5
Q

what things does a CBT therapist help a client to do

A

¥ Identify thoughts, feelings and behaviours
¥ Assess whether thoughts are unrealistic / unhelpful (question own thoughts)
¥ Identify what can change
¥ Confront their fears – with preparation

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6
Q

what type of therapy gives out homework

A

CBT - client must be motivated

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7
Q

what is the evidence behind behavioural activation

A

Evidence that activities function as avoidance and escape from aversive thoughts, feeling and external situations

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8
Q

in behavioural activation, what is the client taught

A

to analyse unintended consequences of their way of responding

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9
Q

what is the lime limit of interpersonal therapy

A

12-16 weeks

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10
Q

what are advantages of interpersonal therapy

A

A grade evidence for treating depression
No formal homework – may be preferable
Client can continue to practise skills beyond the sessions ending

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11
Q

what are limitations of interpersonal therapy

A

Requires degree of ability to reflect – may be difficult for some
Poor social networks – limited interpersonal support to talk about in session

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12
Q

what do patients do in interpersonal therapy

A

construct an interpersonal map
Identify the interpersonal context
Looks at relationships and symptoms
work on focus area

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13
Q

what are the principles of motivational interviewing

A

Express empathy - Understand person’s predicament
Avoid argument - If challenging patient’s position – makes defensive
Support self-efficacy - Patient sets agenda, generates what they might consider changing

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14
Q

what are the 5 stages of change in motivational interviewing

A 
pre- contemplation
contemplation 
planning
action 
maintainging
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15
Q

describe motivational interviewing at each stage of change

A

Pre- contemplation - not much can be done to help
Contemplation – Provide information, risk screening, pros and cons
Planning - Give options for change, build confidence & motivation
Action - Prevent relapsing and give coping strategies, Strategies to maintain goals, encouragement in failures
Maintaining - Coping strategies, weak points, emergencies, slip back protocols

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16
Q

what is the delayed response for many psych meds

A

3-6 weeks

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17
Q

what is the aim when prescribing in psychiatry

A

simplest drug regime
acceptable side effect profile
lowest effective dose

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18
Q

what are indications for anti-depressants

A 
Unipolar and bipolar depression		
organic mood disorders,
schizoaffective disorder			
anxiety disorders including OCD, panic attacks
social phobia
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19
Q

what would you do if the patient is showing no response to anti-depressants after 2 months at an adequate dose

A

switch to another anti-depressant

augment with another

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20
Q

give some classes of anti - depressants

A

Selective Serotonin Reuptake Inhibitors (SSRIs)
Serotonin/Noradrenaline Reuptake Inhibitors (SNRIs)
Tricyclics (TCAs)
Monoamine Oxidase Inhibitors (MAOIs)

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21
Q

how is treatment resistant depression treated

A

Combination of antidepressants e.g. SSRI or SNRI with Mirtazepine
Adjunctive treatment with Lithium
Adjunctive treatment with atypical antipsychotic e.g. Quetipaine, Olanzapine or Aripiprazole
ECT - electroconvulsive therapy,

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22
Q

how does ECT work

A

induced seizure. Slowing dorsal cortex firing

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23
Q

what are side effects of ECT

A

headaches, shorter memory loss

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24
Q

how long should anti-depressants be prescribed after the 2nd episode of depression for prophylaxis

A

2 years

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25
Q

which is the most lethal antidepressant in overdose

A

TCA

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26
Q

what can tricyclics cause

A

QT lengthening

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27
Q

give examples of secondary TCAs

A

Desipramine, notrtriptyline

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28
Q

give example son tertiary TCAs

A

Imipramine, amitriptyline (chronic pain, neuropathic), doxepin, clomipramine

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29
Q

what are some side effects of tertiary TCA

A

antihistaminic (sedation and weight gain), anticholinergic (dry mouth, dry eyes, constipation, memory deficits and potentially delirium), antiadrenergic (orthostatic hypotension, sedation, sexual dysfunction)

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30
Q

what neurotransmitter so secondary and tertiary TCSs work on

A

secondary - noradrenaline

tertiary - serotonin

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31
Q

how do Monoamine Oxidase Inhibitors (MAOIs) work

A

Bind irreversibly to monoamine oxidase in the gut thereby preventing inactivation of amines such as norepinephrine, dopamine and serotonin leading to increased synaptic levels.

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32
Q

why are MAOIs not used in depression

A

side effects and risk of hypertensive crisis

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33
Q

what are some side effects of MAOis

A

orthostatic hypotension, weight gain, dry mouth, sedation, sexual dysfunction and sleep disturbance

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34
Q

when can hypertensive crisis occur with MAOI use

A

taken with tyramine-rich foods or sympathomimetics. *Cheese Reaction!!

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35
Q

when may serotonin syndrome occur

A

if take MAOI with meds that increase serotonin or have sympathomimetic actions

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36
Q

what are symptoms of serotonin syndrome

A

abdominal pain, diarrhea, sweats, tachycardia, HTN, myoclonus, irritability, delirium. Can lead eventually to hyperpyrexia, cardiovascular shock and death.

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37
Q

how do you avoid serotonin syndrome

A

wait 2 weeks before switching from an SSRI to an MAOI.

The exception of fluoxetine where need to wait 5 weeks because of long half-life.

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38
Q

how do SSRI’s work

A

Block the presynaptic serotonin reuptake

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39
Q

what are the most common side effects of SSRIs

A

GI upset, sexual dysfunction, anxiety, restlessness, nervousness, insomnia, fatigue or sedation, dizziness

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40
Q

what symptoms may be seen is SSRI discontinuation syndrome

A

agitation, nausea, disequilibrium and dysphoria

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41
Q

what may be the immediate reaction to SSRIs

A

reaction to increased serotonin in the brain with nausea and more anxious - lead to a better response
insomnia

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42
Q

name some SSRIs

A 
paroxetine
sertraline
fluoxetine
citalopram
escitalopram
fluvoxamine
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43
Q

what is a pro of fluoxetine having a long half life

A

decreased incidence of discontinuation syndromes

good for patients with bad compliance

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44
Q

why is paroxetine goof if there is risk of hypomania

A

short half life - no active metabolites means no build up

45
Q

why is paroxetine given at night

A

sedating properties

46
Q

what are drawbacks of paroxetine

A

o Sedating, wt gain, more anticholinergic effects

o Likely to cause a discontinuation syndrome

47
Q

which SSRI gives the most GI symptoms

A

sertraline

48
Q

what is the biggest risk of citalopram

A

Dose-dependent QT interval prolongation with doses of 10-30mg daily- due to this risk doses of >40mg/day not recommended!

49
Q

what is similar and different between TCAs and SNRIs

A

SNRIs Inhibit both serotonin and noradrenergic reuptake like the TCAS but without the antihistamine, antiadrenergic or anticholinergic side effects

50
Q

name 2 SNRIs

A

venlafaxine

duloxetine

51
Q

why is venlafaxine good for the geriatric population

A

fast renal clearance

52
Q

what is a major con of venlafaxine

A

Can cause a 10-15 mmHG dose dependent increase in diastolic BP.
May cause significant nausea, primarily with immediate-release (IR) tabss
mAny sexual side effects

53
Q

name 2 novel antidepressants

A

mirtazapine

buproprion

54
Q

what are side effects of mertazapine (novel antidepressants )

A

o Increases serum cholesterol by 20% in 15% of patients and triglycerides in 6% of patients
o Very sedating at lower doses. At doses 30mg and above it can become activating and require change of administration time to the morning.
Increases appetite - weight gain (particularly at doses below 45mg

55
Q

what are indications to prescribe mood stabilisers

A

Bipolar, cyclothymia, schizoaffective

56
Q

what classes of drugs are used as mood stabilisers

A

Lithium, anticonvulsants, antipsychotics

57
Q

what is the only medication proven to reduce suiceide rate

A

lithium

58
Q

what is the gold standard drug for major depression

A

lithium

59
Q

what factors predict positive response to lithium

A

o Prior long-term response or family member with good response
o Classic pure mania
o Mania is followed by depression

60
Q

what should you do before starting a patient of lithium

A

Get baseline U&E and TSH

women - pregnancy test

61
Q

how should you monitor someone on lithium

A

Steady state achieved after 5 days- check 12 hours after last dose.
Once stable check q 3 months and TSH and creatinine q 6 months.

62
Q

what is the goal blood level of lithium

A

0.6- 1.2

63
Q

what anomaly associated with lithium makes it teratogenic

A

Ebstein’s anomaly - cardiac

64
Q

what are the most common side effect of lithium

A

GI distress including reduced appetite, nausea/vomiting, diarrhea
hypothyroidism
non significant leukocytosis
o Hair loss, acne
o Reduces seizure threshold, cognitive slowing, intention tremor

65
Q

what are signs of mild lithium toxicity (1.5-2)

A

watch for vomiting, diarrhoea, ataxia, dizziness, slurred speech, nystagmus

66
Q

what are signs of moderate lithium toxicity (2-2.5)

A

nausea, vomiting, anorexia, blurred vision, clonic limb movements, convulsions,
delirium, syncope

67
Q

what are signs of severe lithium toxicity (>2.5)

A

generalized convulsions, oliguria, renal failure, death

68
Q

what antipsychotics are licensed in bipolar

A 
Aripiprazole
Risperdone
Quetiapine
Quetiapine XR
Olanzapine
69
Q

what are anxiolytics used to treat

A

panic disorder, generalized Anxiety disorder, substance-related disorders and their withdrawal, insomnias and parasomnias. I

70
Q

what are anxiolytics often paired with to treat anxiety

A

SSRI/ SNRI

71
Q

name 2 anxiolytics

A

Buspirone (Buspar)

Benzodiazapines

72
Q

what psych conditions are Benzodiazapines sometimes used to treat

A

insomnia, parasomnias and anxiety

CNS depressant withdrawal protocols ex. ETOH withdrawal

73
Q

how do benzodiazepines work

A

Works on GABA receptors to sedate brain, brain becomes used to it so need higher dose, dependence occurs.

74
Q

what are side effects of benzodiazepines

A 
Somnolence		
Cognitive deficits		Amnesia
Disinhibition		
Tolerance			- 
Dependence
75
Q

name 2 benzodiazepines

A

diazepam, lorazepam

76
Q

what is buspirone not used in the acute setting (anxiolytics)

A

Takes around 2 weeks before patients notice results

77
Q

what anti-convulsants are used in treating psychiatric disorders

A

valproic acid
carbamazepine
lamotrigigine

78
Q

what are side effects of lamotrigine

A

o Nausea/vomiting
o Sedation, dizziness, ataxia and confusion
The most severe are toxic epidermal necrolysis and Stevens Johnson’s Syndrome (

79
Q

why should you discontinue lamotrigine immediately if any rash appears

A

risk of steven johnson syndrome / toxic epidermal necrosis

80
Q

what is the first line agent for acute mania and mania prophylaxis

A

Carbamazepine (Tegretol)

81
Q

what should you check before prescribing carbamazepine

A

baseline liver function tests, FBC and an ECG

82
Q

what are side effects of carbamazepine

A

o Rash- most common SE seen
o Nausea, vomiting, diarrhea
o Sedation, dizziness, ataxia, confusion
o AV conduction delays
o Aplastic anemia and agranulocytosis (rare - <0.002%)
o Water retention due to vasopressin-like effect which can result in hyponatremia

83
Q

how is carbamazepine a heteroinducer

A

induces its own metabolism and that of others - contraceptives, warfarin, antidepressants

84
Q

why is valproic acid not first line with bipolar when it is as effective as lithium at mania prophylaxis

A

not as effective in depression prophylaxis.

better tolerance than lithium

85
Q

what are side effects of sodium valproate/ valproic acid

A

o Thrombocytopenia and platelet dysfunction
o Nausea, vomiting, weight gain
o Sedation, tremor
o Increased risk of neural tube defect 1-2% vs 0.14-0.2% in general population secondary to reduction in folic acid. NOT advised for women of child bearing age.
o Hair loss (alopecia)

86
Q

what should you do before prescribing valproic acid

A

baseline liver function tests (lfts), pregnancy test and FBC. Start folic acid supplement in women

87
Q

what are the 4 key pathways affected by dopamine in the brain

A

mesocortical
mesolimbic
nigrostriatal
tuberoinfindivular

88
Q

when are antipsychotics indicated

A

schrizophrenia prophylaxis
low dose bipolar - mood stabilisation/ psychotic features
augmentation in anxiety

89
Q

what can dopamine hypoactivity cause

A

Parkinsonian movements i.e. rigidity, bradykinesia, tremors), akathisia and dystonia

90
Q

what does blocking dopamine in the tuberoinfundibulum pathway predispose a patient to

A

hyperprolactinemia (gynecomastia/galactorrhea/decreased libido/menstrual dysfunction).

91
Q

what is the mechanism of most anti-psychotics

A

dopamine receptor antagonists

92
Q

give examples of low potency anti-psychotics

A

chlorpromazine and Thioridazine

93
Q

give examples of high potency anti-psychotics

A

include Fluphenazine, Haloperidol, Pimozide

94
Q

what side effects are seen in high potency anti-psychotics

A

extrapyramidal and sex side effects

95
Q

what side effects are seen in low potency anti-psychotics

A

more cardiotoxic and anticholinergic adverse effects including sedation, hypotension

96
Q

what is the mechanism of atypical anti-psychotics

A

serotonin-dopamine 2 antagonists (SDAs

97
Q

how long should you put someone on an anti-psychotic before changing

A

8 weeks

98
Q

what is Tardive Dyskinesia (TD

A

involuntary muscle movements that may not resolve with drug discontinuation- risk approx. 5% per year
(anti-psychotics)

99
Q

what is Neuroleptic Malignant Syndrome (NMS)

A

Psychiatric emergency. Characterized by severe muscle rigidity, fever, altered mental status, autonomic instability, elevated WBC, CPK and lfts. Potentially fatal.

100
Q

give examples of Extrapyramidal side effects (EPS):

A

Acute dystonia, Parkinson syndrome, Akathisia, increased suicide

101
Q

what is clozapine received fro

A

treatment resistant schizophrenia

102
Q

what are side effects of clozapine

A

agranulocytosis - weekly blood draws x 6 months, then Q- 2weeks x 6 months)
Increased risk of seizures
Associated with the most sedation, weight gain, hyperlipidaemia and abnormal LFT’s
Increased risk of hypertriglyceridemia, hypercholesterolemia, hyperglycemia,

103
Q

what is a major drawback of olanzapine + Quetiapine (atypical anti-psychotic)

A 
weight gain (30-50lb)
hypertriglyceridemia, hypercholesterolemia, hyperglycemia
104
Q

which atypical antipsychotic has a unique mechanism

A

Aripiprazole - action as a D2 partial agonist

105
Q

what baseline blood work would you do before antipsychotics>

A

Fasting lipid profile. Fasting blood sugar, Lfts, CBC

106
Q

what is a common side effect of siperidone (atypical antipsychotic)

A

akathisia

increases risk of suicide

107
Q

is the first presentation of bipolar is manic, what mood stabiliser will she do better on

A

lithium

108
Q

what is a common blood finding of pateitns of anticonvulsants

A

increased LFTs

up to 3x don’t change

psychiatry (5 decks)

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